Laboratory research was performed to understand leadership by attempting to link EEG baseline frequency patterns with data from the Leadership Opinion Questionnaire (LOQ) assessment survey. Research began with 293 right-handed males, 18 to 26 years-old, who completed the LOQ. Based on their scores, 61 subjects, grouped by the Ohio State Leadership Quadrants, were tested using brain-mapping technology.

Of the three major cell types in bone, osteocytes are considered the major mechanosensors, capable of detecting whole-bone mechanical forces at a cellular level and coordinating tissue-level bone formation and resorption responses. The pathology of age-induced bone loss, a major factor in the development of osteoporosis, is attributed to impaired osteocyte mechanosensing. However, real-time evidence of immediate osteocyte responses to mechanical load to support the blunted tissue-level responses that have been demonstrated thus far is lacking. A ubiquitous cellular response upstream of many functions in all cell types, intracellular calcium (Ca2+) is an early mechanosensitive signal in osteocytes, wherein the response characteristics studied in systems of multiple scales are related to mechanical stimuli. Thus, this phenomenon can be characterized as a real-time measure of osteocyte mechanosensitivity. The objective of this thesis was to utilize an ex vivo model of osteocyte Ca2+ signaling to investigate potentially altered mechanosensitivity of the osteocyte network in two clinical contexts: aging, and a recently-approved therapy for treatment of osteoporosis. Additionally, we aimed to enhance this ex vivo model to identify a functional consequence of this robust Ca2+ signaling response to mechanical load in the context of osteocyte mechanotransduction. We first sought to characterize and compare Ca2+ signaling responses to mechanical load in osteocytes from aged and young-adult mice using an ex vivo model to visualize cell networks in viable mouse tibiae. We found that fewer osteocytes responded to whole-bone cyclic mechanical loading in aged mice tibiae compared to those from young-adult mice and did so in a delayed manner, suggesting a diminished mechanosensitivity to load. Osteocytes from aged mice also lacked the well-correlated relationship between Ca2+ signaling synchrony and cell-cell distance exhibited by young-adult osteocyte networks. Taken together, we have demonstrated, for the first time, a real-time measure of the dampened mechanosensing and lack of signal coordination in aged osteocyte networks in situ, which may contribute to blunted long-term bone formation responses to load. Next, we utilized the ex vivo Ca2+ signaling model to investigate the effect of bone formation in response to treatment with sclerostin antibody (Scl-Ab) on osteocyte mechanosensing. Previous studies have identified two phases of bone formation response to Scl-Ab treatment: an initial period of rapid bone formation with short-term dosing and a return to a steady phase of bone formation response with long-term dosing. Thus, we treated mice according to three groups: vehicle, short-term Scl-Ab, and long-term Scl-Ab. Serum P1NP assays and biweekly micro-CT scans throughout the treatment period confirmed the two phases of bone formation response to Scl-Ab. At the conclusion of treatment, under ex vivo whole-bone loading matched at 10 N, there were no significant differences in osteocyte Ca2+ signaling parameters between treatment groups. However, under strain-matched loading, fewer osteocytes from the short-term group exhibited Ca2+ responses and the initiation of Ca2+ signaling was delayed. We interpreted this as reduced mechanosensing in osteocytes that have been newly-embedded in bone that has been rapidly formed in response to Scl-Ab, as confirmed by alizarin red intensity analysis in the osteocyte field of view ex vivo. This study provides real-time evidence of the cellular responses under the distinct phases of bone formation response to Scl-Ab and demonstrates that osteocyte mechanosensing is maintained with long-term treatment, suggesting that other mechanisms may be responsible for self-regulation of bone formation. Given the robust Ca2+ responses to load characterized in osteocytes by our group and others, we concluded this work by investigating a consequence of this mechanism that may contribute to osteocyte mechanotransduction. A common Ca2+-dependent mechanism that has been demonstrated in osteocytes in vitro with possible implications for cell-cell communication is contraction of the actin cytoskeleton. Therefore, we sought to confirm this mechanism in osteocytes maintained in their native 3D network and morphology using the ex vivo murine tibia model. We successfully enhanced the model to simultaneously image intracellular Ca2+ and the F-actin network of individual osteocytes in situ at high magnification using transgenic Lifeact mice paired with either Ca2+ dye or bred with Ca2+ indicator mice. In both models, using biochemical stimuli, we quantified actin network dynamics over time and identified Ca2+-dependent contractile events. Under mechanical loading, phasic actin network contractions corresponded to individual Ca2+ peaks in single osteocytes. The mechanosensitive nature of these contractions was demonstrated by comparing cellular dynamics in single cells under two paired mechanical loading levels; interestingly, mechanosensitivity was dependent on the order of application of these load magnitudes. In identifying this novel mechanosensitive Ca2+-dependent mechanism, we enhance the understanding of the mechanotransduction pathway in osteocytes and have provided a potential point of intervention in cases where osteocyte mechanotransduction is inhibited, such as in osteoporosis. Taken together, this body of work contributes to knowledge of how osteocytes are sensing mechanical forces in different contexts and transducing signals to effector cells. We provide novel, real-time, immediate measures of osteocyte mechanosensing in situ that may correspond to whole-bone responses, such as age-induced bone loss or the differential responses to Scl-Ab treatment. Future work will focus on ways to recover diminished osteocyte mechanosensing and further connect the cell responses we observe herein to long-term bone formation responses in clinical applications.

The present study examined whether and to what extent physiological rhythms of long-term . night workers become adapted to their unconventionally scheduled hours of work and sleep and how the degree of adaptation would be reflected in ratings of sleep quality, mood, anxiety, energy and satisfaction.

This thesis presents two separate experiments concerning aerobic and anaerobic amphibian energetics. The first study (Part I) investigates differential alterations in the kinetics of the anaerobic enzyme lactate dehydrogenase, in nine species of anurans with varying natural histories. The second study (Part II) studies changes in different anaerobic and aerobic physiological parameters in a single species (Rana catesbeiana) after six weeks of chronic exercised, unexercised-captive and for field frogs. The common theme of these two experiments involves the potential for physiological changes due to environmental stress. Part I examines different species to infer a possible evolutionary relationship to environmental stresses at the molecular level of lactate dehydrogenase. Part II comprises the effects on captivity on aerobic and anaerobic capacities of R. catesbeiana,

The relationship between training intensities and fitness gains was selected as a topic for analysis in this study. Forty-six college men served as subjects in one of three groups: a jogging, or moderate intensity, training group, a running, or high intensity, training group, or a control group. All subjects were pre- and post-tested on the Astrand Bike Ergometer Work Test where working heart rates were measured and recorded. The two training groups participated in at least thirteen training sessions between these testing days, in which two miles were covered at the correct intensity level for each subject at each training session. A review of the literature revealed that most researchers embraced the concept of a minimal threshold of training stimulus needed to be met or exceeded by subjects for significant cardiovascular fitness gains to occur. Conclusions about the absolute level of this threshold varied from a low of 120 heartbeats per minute to at least 150 heartbeats per minute, depending apparently upon the experimental evidence each researcher had gathered. The author hypothesized that there existed a continuum of training stimuli such that training at higher intensities would produce larger heart rate decrements (a cardiovascular fitness index) than at moderate training intensities, but that moderate intensities would also produce significant gains. Furthermore, wide variations in heart rate decrements were expected to be observed within any one group, possibly indicating differences in initial fitnesses of subjects. The factual results of the study were: Both experimental groups and the control group exhibited significant decrements in heart rates from pre-test to post-test although the experimental groups' gains were significant at a higher confidence level. Explanations were posited about the possible factors which might have unpredictably caused the control group to have shown significant improvement. The moderate intensity training group exhibited a larger decrement in heart rate than the high intensity training group, although the difference was not statistically significant. There, indeed, was a wide variation of heart rate responses among individuals within any one group, possible indicating initial fitness differences. In light of the results derived from this study, the author can only conclude: Significant decreases in submaximal workload heart rates may be expected to be observed in American college men after training at moderate to high intensity levels (150 beats per minute or higher) for relatively short training periods (two days per week for eight weeks). Large fluctuations in fitness responses among subjects within any one training group can be expected, due probably to individual differences in initial fitnesses. The task of training large numbers of subjects at specified intensity levels within a fairly realistic physical education setting seems to have been a fruitful approach.

The purpose of the present study was to determine the acute effects of strenuous exercise on the following blood constituents: total cholesterol (TC) 1 triglycerides (TG) 1 high density lipoproteins (HDL-C) 1 and low density lipoproteins (LDL-C). A single case study was performed during a 20 day testing period. Two century bicycle rides ( 100 miles) were used as the strenuous exercise bouts. Blood samples were drawn each day and immediately after each 100 mile ride. A pre-set exercise and diet regimen were followed every day of the 20 day procedure. A t-test upon TC 1 TG 1 HDL-C 1 and LDL-C was done to determine the statistical significance between two 100 mile cycling rides and the training days. The change upon TC was an increase of 11.1mg/dl and the change upon TG was an increase of 66.8mg/dl. The t-tests upon both of these variables were found to be significant at the <0.05 level. The change upon HDL-C was an increase of 3.2mg/dl but a ttest showed no statistical significance at the <0.05 level. The change upon LDL-C was a decrease of 2.6mg/dl but a t-test showed no statistical significance at the <0.05 level. Total cholesterol to HDL-C ratio (TC/HDL-C) did not change and a t-test showed no statistical significance at the <0.05 level. The ratio stayed at 2.5 for the duration of the study period. It was determined that an acute bout of exercise significantly changed TC and TG levels. Total cholesterol mean values changed from 106.4mg/dl ± 1.11 to 117.5mg/dl ± 3. 53. Mean TG values changed from 66. 2mg/dl ± 4. 08 to 113mg/dl ± 16.97. The acute bout of exercise did not significantly change HDL-C or LDL-C. possibilities are discussed.

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